1. Oesophagus and Stomach
Phil Thirkell + asfand baig

2. Anatomy Blood supply to the oesophagus and stomach?
Coeliac artery – a branch off the abdominal aorta
Which embryonic structure does the oesophagus derive from?
Foregut
Endoderm

3. Histology Cell Type Non- Keratinised Stratified Squamous Epithelium
Upper 1/3 oesophagus
Striated muscle
Middle 1/3 oesophagus
Striated muscle and Smooth muscle
Lower 1/3 oesophagus
Smooth muscle

4. Smooth Muscle
Narrow, rod shaped cells
No striations
One nucleus per cell
Striated Muscle
Tubular cells
Striations
Multiple nuclei

5. Gastro-oesophageal Junction
How can you tell where the junction is?
Change from non-keratinised stratified squamous to simple columnar
What forms the lower oesophageal sphincter?
Compression from the diaphragm (right crus)
Angle of entry into the stomach
Intra-abdominal pressure
Mucosal folds (but I don’t know how these help form the junction)

6. Pathology Gastro-Oesophageal Reflux Disease Barrett’s Oesophagus
Failure of lower sphincter causes reflux of acid
Oedema/white cell infiltration
Increases risk of cancer
Barrett’s Oesophagus
Metaplasia from stratified squamous to simple columnar
Goblet cells
Produce mucus to protect against acid environment
Considered a pre-malignant condition
Association with adenocarcinoma
Oesophageal Cancer
Late presentation
Can cause obstruction
Poor prognosis
Risk Factors:
Age, male, FH, smoking, alcohol, reflux, Barrett’s, hot drinks
Oesophageal Varices
Dilated veins of portal system
Form due to portal hypertension
Risk of bleeding
Difficult to treat

7. Stomach Functions of the stomach? What are the folds in the stomach?
Storing food
Killing bacteria
Regulate food entry into duodenum
Dissolve and partially digest macromolecules into food
To secrete intrinsic factor
the only indispensable role of the stomach
What are the folds in the stomach?
Rugae – same name for the folds in the bladder, which do the same – allow increase in size without increasing the pressure within

8. Stomach Anatomy

9. Stomach Secretions Contents of stomach secretions? Chief cell
Hydrochloric acid
Enzymes – pepsinogen, gastric lipase
Mucus
Bicarbonate
Water
Intrinsic Factor
Chief cell
Pepsinogen
Parietal cell
HCl
G-cell
Gastrin
Mucus cell
Mucus
D-cell
Somatostatin
ECL-cell
Histamine
Histamine and Gastrin – stimulate acid secretion
Somatostatin – inhibits gastrin/acid secretion

10. Parietal Cell

11. Stimulation of Acid Secretion
Stimulates acid secretion
Inhibits acid secretion
Histamine
Somatostatin
Gastrin
Prostaglandins
Acetylcholine
Enteric hormones - VIP

12. Dysphagia difficulty swallowing Disease of mouth/tonsils
Inflammation or cancer
Stricture
Pharyngeal pouch
Hiatus hernia
Achalasia – problem with peristalsis co-ordination. (sorry to those I told wrong, I was getting confused with oesophageal atresia)
Goitre
Infections (oesophagitis)
Aortic aneurysm

13. Peptic Ulcer Causes: Helicobacter pylori NSAIDs Crohn’s disease Cancer
Zollinger-Ellison syndrome
A non-beta islet cell, gastrin-producing tumour of the pancreas. Loads of gastrin causes huge acid secretion all the time, making patients really prone to ulcers
Urease enzymes
Break down urea into CO2 and ammonia. The ammonia then neutralises the stomach acid, allowing bacteria to survive more readily.
How to test for H.pylori?
Urease breath test
Blood antibody serology
Biopsy and urease test
Stool antigen

14. Peptic Ulcer Epigastric pain – what happens on eating? Nausea
A gastric ulcer gets worse on eating. Food enters stomach, acid is released and it comes into contact with the ulcer, aggravating it and causing pain.
A duodenal ulcer is made better on eating as the pyloric sphincter closes and bicarbonate is released from the pancreas. The pain then starts again after 2-3 hours when the contents of the stomach is released and the acid comes into contact with the ulcer.
Nausea
Bloating/flatulence
Epigastric tenderness
Anaemia – chronic bleeding from the ulcer

15. Why do NSAIDs cause ulcers?
Normally, prostaglandins are released when gastric mucosa is damaged, causing increased production of mucus and bicarbonate.
Cyclo-oxygenase enzyme 1 (COX-1) creates prostaglandins.
NSAIDs inhibit COX-1, reducing prostaglandin production. This decreases the mucus and bicarbonate secretion
This increases the damage by acid on gastric mucosa  ulcers

16. Stomach Pharmacology Antacids Alginates Bismuth chelates
Prostaglandin analogues
H2 antagonist
Proton pump inhibitors
H. pylori eradication therapy

17. Antacids
React chemically to neutralise stomach acid (acid + base  salt + water + carbon dioxide)
Magnesium hydroxide
Calcium Carbonate
e.g. Rennie
S/E - gas

18. Alginates
Polysaccharide which reacts with stomach contents to make a raft which floats on the surface to prevent reflux and protects mucosa
E.g. Sodium alginate
Gaviscon is combined antacid and alginate

19. Bismuth Chelates Binds pepsin to prevent acid secretion
Coats the mucosa
Increases prostaglandin production
S/E – can cause black tongue and black faeces

20. Prostaglandin Analogues
Misoprostol
Inhibits acid secretion
Increases mucosal blood flow to generate HCO3
S/E: diarrhoea and stomach cramps
Can’t be used in pregnancy – causes uterine contractions and can cause a termination
women of child-bearing age should be using contraceptives if prescribed misoprostol as gastric acid treatment

21. H2-receptor antagonists (anti-histamines)
Blocks the histamine receptor on the parietal cell to reduce acid secretion
e.g. Cimetidine, ranitidine, nizatidine
(not loratidine – only blocks H1, so used in allergies)

22. Proton Pump Inhibitors
e.g. omeprazole, lansoprazole, pantoprazole
Block the H+/K+-ATPase pump of the gastric parietal cell
Used in patients with reflux, GORD, NSAID ulcers and as 2° prevention in pts who’ve had ulcers
Used to control Zollinger-Ellison until something else can be done about it
Acts systemically, in that it is absorbed into the blood stream, circulates and then acts on the parietal cells – instead of just acting directly on them in the stomach lumen
In acidic conditions the drug can bind to the ATPase, but in neutral conditions it cant.
S/E - ↑risk of infection due to ↓ acid secretion to kill bacteria, decreased vitamin B12 absorption due to less acid, decreased calcium absorption.
Nausea + vomiting

23. H. Pylori eradication 1 week of:
1 proton pump inhibitor – omeprazole, lansoprazole
2 antibiotics – amoxicillin and either: clarithromycin or metronidazole
Can’t use serology to check if the eradication therapy has worked because the antibodies will still be there even if all the bacteria are now dead
To help remember:
--Need 2 antibiotics because it could be resistant to one of them
--Only 1 PPI because no resistance to them and they work really well